NDLI: Crohn’s Disease-Associated Nod2 Mutation Limits Production of Pro-Inflammatory Cytokines to Protect the Host from Enterococcus faecalis-Induced Lethality 1

Content Provider	PubMed Central
Author	Kim, Yun-gi Shaw, Michael H. Warner, Neil Park, Jong-hwan Chen, Felicia Ogura, Yasunori Núñez, Gabriel
Abstract	Nod2 mutations including L1007fsinsC are associated with the development of Crohn’s disease (CD). These CD-associated Nod2 mutations are common in healthy Caucasian populations, suggesting that they may confer some protective function, but experimental evidence is lacking. Using a mouse strain that expresses Nod22939iCstop, the equivalent of the L1007fsinsC mutation, we found that macrophages homozygous for Nod22939iCstop are impaired in the recognition of MDP and E. faecalis, a commensal bacterium that is a common cause of sepsis-associated lethality in humans. Notably, Nod2 deficiency and homozygocity for Nod22939iCstop were associated with reduced production of TNF-α and IL-6 and lethality after systemic infection with E. faecalis despite normal bacteria loads. Consistently, inhibition of TNF-α Signaling protected wild-type mice from E. faecalis-induced lethality. These results suggest that the same Nod2 mutation can increase the susceptibility to CD, but also protect the host from systemic infection by a common enteric bacterium.
Related Links	http://dx.doi.org/10.4049/jimmunol.1001854
Ending Page	2852
Page Count	4
Starting Page	2849
File Format	PDF
ISSN	00221767
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	6
Volume Number	187
Language	English
Publisher Date	2011-09-15
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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